Biomedical subjects

L Y Hu

Publications and source records attributed to L Y Hu.

33 records · Page 2Linked to original sources

PubMed1992

Spectrofluorimetric determination of tetracycline and anhydrotetracycline in serum and urine.

A spectrofluorimetric method, involving alkaline degradation and formation of a magnesium complex, is described for the determination of tetracycline (TC) and anhydrotetracycline (ATC) in their mixed solution. Tetracycline is degraded and determined in alkaline solution. This treatment of ATC produces almost no fluorescence, but a fluorescent magnesium complex forms at pH 7.5. Several synthetic samples of TC and ATC, with TC:ATC ratios ranging from 50:1 to 1:50, were analysed. The recoveries of TC and ATC are about 71-76 and 61-63% in serum, respectively, and are all about 100% in urine.

Humans↗

PubMed1992

New CNS-specific calcium antagonists.

Ischemic insults to the brain in stroke or traumatic brain injury produce excessive release of glutamate from depolarized nerve terminals. This excessive glutamate release in turn stimulates massive calcium entry into nerve cells, activating a biochemical cascade that results in cell death. A major pathway of calcium entry into depolarized nerve cells is through voltage-sensitive, high threshold calcium channels. A large fraction of this calcium entry is mediated through "R-type" calcium channels, channels resistant to blockage by dihydropyridine calcium antagonists such as nimodipine. A newly discovered compound derived from spider venom, CNS 2103, antagonizes both R-type channels and dihydropyridine-sensitive ("L-type") calcium channels. This broad spectrum of action, coupled with selectivity for calcium channels over other classes of voltage-sensitive and ligand-gated ion channels, makes CNS 2103 an interesting lead for development of drugs to treat ischemic brain injury. Activation of presynaptic ("N-type") calcium channels in nerve terminals is a primary cause of excessive neurotransmitter release in brain ischemia. Prevention of glutamate release by blockade of N-type channels in glutamatergic nerve terminals may, at an early stage in the pathophysiological cascade, abort the process leading to nerve cell death. Cambridge NeuroScience has developed a novel rapid kinetic approach for monitoring glutamate release from brain nerve terminals in vitro, and this has led to CNS 1145, a substituted guanidine that selectively blocks a kinetic component of calcium-dependent glutamate release mediated by persistent depolarization. Additional evidence suggests that CNS 1145 antagonizes presynaptic N-type calcium channels, and this may account at least in part for its ability to block glutamate release.

Animals↗

PubMed1990

Inhibition of cathepsin B and papain by peptidyl alpha-keto esters, alpha-keto amides, alpha-diketones, and alpha-keto acids.

A series of peptidyl alpha-keto esters, alpha-keto amides, alpha-keto acids, and alpha-diketones were synthesized which reversibly inhibit papain and cathepsin B. Methyl 3-(N-benzyloxycarbonyl-L-phenylalanyl)amino-2-oxopropionate (a dicarbonyl compound) inhibits papain with a Ki value of 1 microM, whereas the Ki of 3-(N-acetyl-L-phenylalanyl)aminopropanone (a monocarbonyl compound) is 1.5 mM (M. R. Bendall et al., 1979. Eur. J. Biochem. 79, 201-209). Both carbonyl groups are required for effective inhibition. Extension of these inhibitors by addition of P substituents (e.g., hexyl) does not affect the Ki for papain, but reduces Ki for cathepsin B 33-fold. For these two enzymes slow binding inhibition was observed with slow on rates (kappa on, 5.2 X 10(2) M-1 s-1 for papain, and 2.7 X 10(3) M- s-1 for cathepsin B). Addition of a P3 substituent (glycine) has no effect on Ki. We propose that the mechanism of inhibition involves the formation of a hemithioketal by addition of the active-site thiol to the carbonyl group of the inhibitor closer to the N-terminus. The hemithioketal intermediate is most likely stabilized by the electron withdrawing effect of the second carbonyl group.

Amides↗

PubMed1989

Imaging diagnostic value of myxoma in cardiac chamber. An analysis of 23 cases.

Twenty-three patients with myxoma in the cardiac chamber were analysed from their clinical manifestations and imaging diagnoses. All the patients were confirmed pathologically and 22 of them were further confirmed by operation. In this series, 18 patients had the tumors in the left atria, 3 in the right atria, and 2 in the right ventricles. Diagnosing myxoma by CT and two-dimensional echocardiography was evaluated. The results suggest that to diagnose myxoma in the cardiac chamber, CT is as effective as sonography because it can display clear image, precise location and mobility of the tumor with the flowing blood stream in the cardiac chamber, and provide reliable indications for surgery.

Adolescent↗

PubMed1989

Viral etiology of cervical carcinoma. Human papilloma virus and herpes simplex virus type 2.

The possible role of human papilloma virus (HPV) and herpes simplex virus type 2 (HSV-2) in the viral etiology of cervical carcinoma was investigated a series of cervical lesions were studied for the presence of HPV and HSV-2 DNA sequences as well as HPV and HSV-2 antigens by DNA dot blot hybridization technique and high-specificity PAP staining method. The results obtained were correlated with the histologic diagnosis. HPV 16 DNA sequences detected in cervical carcinoma biopsies were 43%, whereas HSV-2 DNA sequences were only 8%. HPV antigens detected in cervical dysplasia were 31%, whereas those detected in cervical carcinoma and cervicitis were the least. HSV-2 antigens were detected in chronic cervicitis, dysplasia and cervical carcinoma. The difference in positive rate between the cervical carcinoma and cervicitis groups was statistically significant, (chi-square test, P less than 0.01). No HPV DNA and HSV-2 DNA sequences were found in the same specimen, although both HPV DNA sequences and HSV-2 antigens were found in the same sample in some cases. The results indicate that the viral etiology of cervical carcinoma may be multifactorial. Both HSV-2 and HPV may be associated with cervical carcinoma, but the mechanisms involved are different. HSV-2 and HPV may act synergistically in the development of cervical carcinoma.

Antigens, Viral, Tumor↗

PubMed1988